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The NCBI web psoriazis Kirov requires JavaScript to function. It is generally accepted that the pathogenesis of psoriasis involves accumulation of effector T-cells within lymph nodes and their subsequent migration into the skin through the blood system. Here we provide evidence that psoriatic plaque itself may serve as a source of inflammatory T-cells. Skin samples were obtained from 41 patients with progressive psoriatic lesions; 18 of these patients also donated skin specimens during the remission of the disease.

The control group consisted of 16 healthy subjects. The observed differences demonstrated high level of statistical mit Lemon in psoriazis Thrombosen. Progressive phase of psoriasis psoriazis Kirov characterized by intradermal proliferation of T-cells.

This model is perfectly compatible with the primary immune response observed at the onset of the disease, e. Indeed, the development of psoriasis frequently involves inflammation psoriazis Kirov the pharyngeal lymphoid ring caused by β-hemolytic streptococcus. The latent period of weeks is required for the maturation of effector T-cells and hematogenous dissemination of these cells, as evidenced by multifocal lesions.

However, the above model fails to explain some aspects of the disease relapse. For example, the recurrence of plaques is usually observed on psoriazis Kirov same "favorite" sites, suggesting the existence of topical immunological memory within the skin. Surprisingly, regional lymph nodes always remain intact, irrespectively of the severity of psoriatic relapse.

Altogether, these observations put into the question ale umăr în mâncărimi pielii exclusive role of lymph nodes in producing effector T-cells. We hypothesized that the psoriatic psoriazis Kirov itself may serve as a source of antigen-specific T-cells.

Psoriazis Kirov report provides evidence to support this assumption. The study included 41 patients with active psoriasis vulgaris mean age Punch biopsies 6 mm source obtained from the periphery of psoriatic plaques. Control samples psoriazis Kirov 16 healthy individuals included the material leftover after plastic surgeries mean age All recruited subjects were required to sign an informed consent form.

The antibodies used for immunohistochemistry are listed in table 1. The article source analysis salitsilovo- zinc psoriazis unguent assisted by the "UTHSCSA ImageTool 3. Based on the obtained data, median count of positive cells per field was calculated. Statistical analysis was performed using tălpi psoriazis IBM SPSS Statistics, version Wilcoxon-Mann-Whitney test was used to evaluate the differences between the psoriazis Kirov of the skin from progressive psoriatic lesions, remission of psoriasis and healthy individuals.

A p -value of less than 0. In addition, abundant Ki67 staining was detected in keratinocytes of psoriazis Kirov basal and lower spinous layers of the epidermis of progressive psoriatic lesions Figure 1. As expected, the number of proliferating Kipositive cells was significantly higher in the derma samples from the patients psoriazis Kirov progressive psoriatic lesions compared with samples from the patients in remission; meanwhile, the derma of healthy individuals contained very psoriazis Kirov scattered Ki67 positive cells Table 2Figure 1.

No proliferating T-cells were detected in the skin of healthy individuals Figure 1. The skin of patients with psoriasis in remission contained just single proliferating T-cells.

Thus, the obtained data suggest that proliferation of T-cells in psoriatic patients does not necessarily involve lymph node tissue, but can occur directly in the progressive psoriazis Kirov lesions.

Therefore, the skin of psoriatic patients can operate as a lymphoid organ. These results do not conflict with the literature data. Local activation of T-cells is considered to be an important feature of psoriatic skin lesions. Pro-inflammatory cytokine IL17A, being psoriazis Kirov by Th17 cells, is capable to initiate the formation of ectopic lymphoid organs upon chronic inflammation. The formation of the ectopic foci of lymphoid tissue, which resemble lymphoid follicles, is characteristic link the psoriazis Kirov suffering from chronic inflammation.

These foci are usually referred to as tertiary lymphoid organs TLO. Unlike the lymph nodes, TLO are not encapsulated and therefore engaged in direct interaction with the neighboring tissues. TLO are a landmark of many autoimmune diseases and related conditions, being observed in inflammatory tissues from patients with rheumatoid arthritis, Hashimoto's thyroiditis, recipients of transplanted organs, etc.

Our psoriazis Kirov suggest that the formation of the cellular infiltrate in the skin of psoriazis Kirov with psoriasis may occur not only through migration of the immune cells from the peripheral blood, but also by intradermal T-Cell proliferation.

These memory T-cells may psoriazis gravide în fotografii silent for some periods of time, but become activated upon various stimuli and trigger the development of psoriatic lesion. The existence of the intradermal memory T-Cell explains why psoriatic plaques almost always relapse at the sites of the previously regressed lesions. Therapeutic psoriazis Kirov of the specific populations of silent intradermal T-cells appears to be a promising approach for prolonging remission of the disease in psoriatic patients.

Russian Foundation for Psoriazis Kirov Research grantsand National Psoriazis Kirov for Biotechnology InformationU.

METHODS Skin samples were obtained from 41 patients with progressive psoriatic lesions; 18 of these patients also donated skin specimens during the remission of the disease. Cell proliferation, Psoriasis, T-Lymphocytes. Psoriazis Kirov Patients and biopsies The study included 41 patients with active psoriasis vulgaris mean age Antibodies and immunohistochemistry The antibodies used for immunohistochemistry are listed in table 1.